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Brain Sciences
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Cellular and Molecular Basis of Neurodegenerative Disease
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Cellular and Molecular Basis of Neurodegenerative Disease

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (5 October 2023) | Viewed by 16329

Special Issue Editor

Dr. Deepshikha Pande Katare

E-Mail Website
Guest Editor
Amity Institute of Biotechnology, Amity University Uttar Pradesh, Noida 201313, India
Interests: medical biotechnology; proteomics for biomarker discovery in hepatocellular carcinoma; lung cancer; neurodegenerative diseases; type III diabetes; novel drug delivery & drug targeting in cancer; Alzheimers; Parkinson’s; epilepsy; type II & III diabetes

Special Issue Information

Dear Colleagues,

Neurodegeneration is the progressive degradation of specific neurons caused by as-yet unidentified cellular and molecular pathogenic mechanisms. Only symptomatic management drugs are available because they do not address the underlying cause of the disorder. There are currently no treatments to either cure or halt the progression of the pathology. To find new molecular targets and create efficient treatments to treat and/or prevent these terrible diseases, it is crucial to comprehend the molecular underpinnings of neurodegenerative disorders. The past decade witnessed various novel research wherein the multi-organ role in neurodegenerative diseases was highlighted. For example- there is growing evidence that the gut microbiota and their metabolites produced via gut microbiome influence brain health. Also, gut-derived nutrients and other signals are delivered to the liver via the portal circulation. The crosstalk between the gut/liver-brain axis is increasingly recognized in neurodegenerative sciences domain which is further strengthened by the parallel rise in liver diseases and gastrointestinal and immune disorders.  

This Special Issue intends to publish original and/or review articles addressing the state of the art and scientific viewpoints on this topic. We are seeking authors to submit manuscripts exploring the pathogenic commonalities and differences among neurodegenerative disorders. We are also seeking novel prospects for molecular targets, biomarkers, gut-liver-brain axis pathophysiology and therapeutics, We are interested in underlying mechanisms representing the genetics, cell biology, pathology and biochemistry of the neurodegenerative disorders, including Parkinson’s, Alzheimer’s, ALS, prion disease, frontotemporal dementia and Huntington’s disease. Innovative study models, such as neurons produced from iPSCs and brain organoids, are also welcome. Authors are encouraged to contribute both original and review papers associated with but not limited to the subjects mentioned here.

Dr. Deepshikha Pande Katare
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegenerative disorder
  • molecular mechanism
  • novel therapeutics
  • target site drug delivery
  • pharmacodynamic biomarkers
  • cell-signaling
  • synergistic approach in therapeutics
  • molecular docking
  • gut-brain axis
  • liver-brain axis
  • novel disease animal models

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Published Papers (6 papers)

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Research

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14 pages, 2151 KiB  
Article
Rab Geranylgeranyltransferase Subunit Beta as a Potential Indicator to Assess the Progression of Amyotrophic Lateral Sclerosis
by Jing Yang, Cheng Xin, Jia Huo, Xin Li, Hui Dong, Qi Liu, Rui Li and Yaling Liu
Brain Sci. 2023, 13(11), 1531; https://doi.org/10.3390/brainsci13111531 - 30 Oct 2023
Cited by 1 | Viewed by 1426
Abstract
Background: Currently, there is no effective treatment for amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disorder. Many biomarkers have been proposed, but because ALS is a clinically heterogeneous disease with an unclear etiology, biomarker discovery for ALS has been challenging due to the [...] Read more.
Background: Currently, there is no effective treatment for amyotrophic lateral sclerosis (ALS), a devastating neurodegenerative disorder. Many biomarkers have been proposed, but because ALS is a clinically heterogeneous disease with an unclear etiology, biomarker discovery for ALS has been challenging due to the lack of specificity of these biomarkers. In recent years, the role of autophagy in the development and treatment of ALS has become a research hotspot. In our previous studies, we found that the expression of RabGGTase (low RABGGTB expression and no change in RABGGTA) is lower in the lumbar and thoracic regions of spinal cord motoneurons in SOD1G93A mice compared with WT (wild-type) mice groups, and upregulation of RABGGTB promoted prenylation modification of Rab7, which promoted autophagy to protect neurons by degrading SOD1. Given that RabGGTase is associated with autophagy and autophagy is associated with inflammation, and based on the above findings, since peripheral blood mononuclear cells are readily available from patients with ALS, we proposed to investigate the expression of RabGGTase in peripheral inflammatory cells. Methods: Information and venous blood were collected from 86 patients diagnosed with ALS between January 2021 and August 2023. Flow cytometry was used to detect the expression of RABGGTB in monocytes from peripheral blood samples collected from patients with ALS and healthy controls. Extracted peripheral blood mononuclear cells (PBMCs) were differentiated in vitro into macrophages, and then the expression of RABGGTB was detected by immunofluorescence. RABGGTB levels in patients with ALS were analyzed to determine their impact on disease progression. Results: Using flow cytometry in monocytes and immunofluorescence in macrophages, we found that RABGGTB expression in the ALS group was significantly higher than in the control group. Age, sex, original location, disease course, C-reactive protein (CRP), and interleukin-6 (IL-6) did not correlate with the ALS functional rating scale—revised (ALSFRS-R), whereas the RABGGTB level was significantly correlated with the ALSFRS-R. In addition, multivariate analysis revealed a significant correlation between RABGGTB and ALSFRS-R score. Further analysis revealed a significant correlation between RABGGTB expression levels and disease progression levels (ΔFS). Conclusions: The RABGGTB level was significantly increased in patients with ALS compared with healthy controls. An elevated RABGGTB level in patients with ALS is associated with the rate of progression in ALS, suggesting that elevated RABGGTB levels in patients with ALS may serve as an indicator for tracking ALS progression. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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25 pages, 7442 KiB  
Article
The Connection between Chronic Liver Damage and Sporadic Alzheimer’s Disease: Evidence and Insights from a Rat Model
by Ruchi Jakhmola Mani, Nitu Dogra and Deepshikha Pande Katare
Brain Sci. 2023, 13(10), 1391; https://doi.org/10.3390/brainsci13101391 - 29 Sep 2023
Cited by 2 | Viewed by 2309
Abstract
Junk foods are typically low in essential nutrients, such as vitamins, minerals, and antioxidants. They are also loaded with trans fats and saturated fats, which can increase the level of triglycerides in the blood. High triglyceride levels can contribute to the development of [...] Read more.
Junk foods are typically low in essential nutrients, such as vitamins, minerals, and antioxidants. They are also loaded with trans fats and saturated fats, which can increase the level of triglycerides in the blood. High triglyceride levels can contribute to the development of non-alcoholic fatty liver disease (NAFLD), a condition where excess fat accumulates in the liver. A high intake of junk foods can lead to insulin resistance, a condition where the body’s cells become less responsive to insulin. A diet lacking in nutrients and loaded with unwanted toxins can impair the liver’s ability to detoxify harmful substances and damage its overall function. It is known that the regular consumption of junk food can be linked to memory impairment and cognitive decline. Several studies have shown that diets high in unhealthy fats, sugars, and processed foods can negatively impact brain health, including memory function. In this study, Wistar rats were used to model Late-Onset Alzheimer’s Disease (LOAD), which was inspired by knowledge of the liver–brain axis’s role in causing dementia. The model mimicked junk-food-induced liver–brain damage, and was developed by using the toxins d-galactosamine, ethanol and d-galactose. To begin with, the model rats demonstrated insulin resistance, a characteristic of LOAD patients. Glucose levels in both the brain and liver tissues were significantly elevated in the model, paralleling clinical findings in LOAD patients. High glucose levels in the brain lead to the increased production of advanced glycation end-products (AGEs), which, along with amyloid beta, harm neighbouring neurons. Histopathological analysis revealed deformed glial nodules, apoptotic neurons, and amyloid plaques in the brain section in the later stages of the disease. Simultaneously, the liver section displayed features of cirrhosis, including an effaced lobular architecture and the extravasation of red blood cells. Liver enzymes ALT, AST and ALP were consistently elevated with disease progression. Furthermore, immunohistochemistry confirmed the presence of amyloid precursor protein (APP) in the diseased brain. The positive expression of Hypoxia-Inducible Factor 3-Alpha (HIF3A) in the brain indicated hypoxic conditions, which is consistent with other LOAD studies. This model also exhibited damaged intestinal villi and excessive bowel and urinary incontinence, indicating malnutrition and a disturbed gut microbiome, which is also consistent with LOAD patients. Bioinformatics analysis on serum protein suggests a few affected molecular pathways, like the amyloid secretase pathway, androgen/oestrogen/progesterone biosynthesis, the apoptosis signalling pathway, the insulin/IGF pathway-protein kinase B signalling cascade, the Metabotropic glutamate receptor group I pathway, the Wnt signalling pathway, etc. Behavioural analysis confirmed memory decline and the loss of muscle strength with disease progression. Overall, this rat model of LOAD sheds valuable light on LOAD pathology and highlights the potential link between liver dysfunction, particularly induced by the excessive consumption of junk food, and LOAD. This study contributes to a deeper understanding of the complex molecular mechanisms involved in LOAD, paving the way for new possibilities in therapeutic interventions. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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20 pages, 1433 KiB  
Article
Exploring Whether Iron Sequestration within the CNS of Patients with Alzheimer’s Disease Causes a Functional Iron Deficiency That Advances Neurodegeneration
by Steven M. LeVine, Sheila Tsau and Sumedha Gunewardena
Brain Sci. 2023, 13(3), 511; https://doi.org/10.3390/brainsci13030511 - 18 Mar 2023
Cited by 9 | Viewed by 3094
Abstract
The involvement of iron in the pathogenesis of Alzheimer’s disease (AD) may be multifaceted. Besides potentially inducing oxidative damage, the bioavailability of iron may be limited within the central nervous system, creating a functionally iron-deficient state. By comparing staining results from baseline and [...] Read more.
The involvement of iron in the pathogenesis of Alzheimer’s disease (AD) may be multifaceted. Besides potentially inducing oxidative damage, the bioavailability of iron may be limited within the central nervous system, creating a functionally iron-deficient state. By comparing staining results from baseline and modified iron histochemical protocols, iron was found to be more tightly bound within cortical sections from patients with high levels of AD pathology compared to subjects with a diagnosis of something other than AD. To begin examining whether the bound iron could cause a functional iron deficiency, a protein-coding gene expression dataset of initial, middle, and advanced stages of AD from olfactory bulb tissue was analyzed for iron-related processes with an emphasis on anemia-related changes in initial AD to capture early pathogenic events. Indeed, anemia-related processes had statistically significant alterations, and the significance of these changes exceeded those for AD-related processes. Other changes in patients with initial AD included the expressions of transcripts with iron-responsive elements and for genes encoding proteins for iron transport and mitochondrial-related processes. In the latter category, there was a decreased expression for the gene encoding pitrilysin metallopeptidase 1 (PITRM1). Other studies have shown that PITRM1 has an altered activity in patients with AD and is associated with pathological changes in this disease. Analysis of a gene expression dataset from PITRM1-deficient or sufficient organoids also revealed statistically significant changes in anemia-like processes. These findings, together with supporting evidence from the literature, raise the possibility that a pathogenic mechanism of AD could be a functional deficiency of iron contributing to neurodegeneration. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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Review

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17 pages, 1887 KiB  
Review
REM Sleep Loss-Induced Elevated Noradrenaline Plays a Significant Role in Neurodegeneration: Synthesis of Findings to Propose a Possible Mechanism of Action from Molecule to Patho-Physiological Changes
by Shatrunjai Giri, Rachna Mehta and Birendra Nath Mallick
Brain Sci. 2024, 14(1), 8; https://doi.org/10.3390/brainsci14010008 - 21 Dec 2023
Cited by 1 | Viewed by 2566
Abstract
Wear and tear are natural processes for all living and non-living bodies. All living cells and organisms are metabolically active to generate energy for their routine needs, including for survival. In the process, the cells are exposed to oxidative load, metabolic waste, and [...] Read more.
Wear and tear are natural processes for all living and non-living bodies. All living cells and organisms are metabolically active to generate energy for their routine needs, including for survival. In the process, the cells are exposed to oxidative load, metabolic waste, and bye-products. In an organ, the living non-neuronal cells divide and replenish the lost or damaged cells; however, as neuronal cells normally do not divide, they need special feature(s) for their protection, survival, and sustenance for normal functioning of the brain. The neurons grow and branch as axons and dendrites, which contribute to the formation of synapses with near and far neurons, the basic scaffold for complex brain functions. It is necessary that one or more basic and instinct physiological process(es) (functions) is likely to contribute to the protection of the neurons and maintenance of the synapses. It is known that rapid eye movement sleep (REMS), an autonomic instinct behavior, maintains brain functioning including learning and memory and its loss causes dysfunctions. In this review we correlate the role of REMS and its loss in synaptogenesis, memory consolidation, and neuronal degeneration. Further, as a mechanism of action, we will show that REMS maintains noradrenaline (NA) at a low level, which protects neurons from oxidative damage and maintains neuronal growth and synaptogenesis. However, upon REMS loss, the level of NA increases, which withdraws protection and causes apoptosis and loss of synapses and neurons. We propose that the latter possibly causes REMS loss associated neurodegenerative diseases and associated symptoms. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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18 pages, 1916 KiB  
Review
Unraveling the Multifaceted Role of the Golgi Apparatus: Insights into Neuronal Plasticity, Development, Neurogenesis, Alzheimer’s Disease, and SARS-CoV-2 Interactions
by Corneliu Toader, Lucian Eva, Razvan-Adrian Covache-Busuioc, Horia Petre Costin, Luca-Andrei Glavan, Antonio Daniel Corlatescu and Alexandru Vlad Ciurea
Brain Sci. 2023, 13(10), 1363; https://doi.org/10.3390/brainsci13101363 - 23 Sep 2023
Cited by 1 | Viewed by 2712
Abstract
This article critically evaluates the multifunctional role of the Golgi apparatus within neurological paradigms. We succinctly highlight its influence on neuronal plasticity, development, and the vital trafficking and sorting mechanisms for proteins and lipids. The discourse further navigates to its regulatory prominence in [...] Read more.
This article critically evaluates the multifunctional role of the Golgi apparatus within neurological paradigms. We succinctly highlight its influence on neuronal plasticity, development, and the vital trafficking and sorting mechanisms for proteins and lipids. The discourse further navigates to its regulatory prominence in neurogenesis and its implications in Alzheimer’s Disease pathogenesis. The emerging nexus between the Golgi apparatus and SARS-CoV-2 underscores its potential in viral replication processes. This consolidation accentuates the Golgi apparatus’s centrality in neurobiology and its intersections with both neurodegenerative and viral pathologies. In essence, understanding the Golgi’s multifaceted functions harbors profound implications for future therapeutic innovations in neurological and viral afflictions. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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16 pages, 879 KiB  
Review
Neuroprotective Potential of Flavonoids in Brain Disorders
by Syed Hasan, Nabeel Khatri, Zainab N. Rahman, Amanda A. Menezes, Joud Martini, Faheem Shehjar, Numa Mujeeb and Zahoor A. Shah
Brain Sci. 2023, 13(9), 1258; https://doi.org/10.3390/brainsci13091258 - 29 Aug 2023
Cited by 11 | Viewed by 3435
Abstract
Flavonoids are a large subgroup of polyphenols known to be sourced from over 6000 natural products, including fruits, vegetables, bark, and herbs. Due to their antioxidant properties, flavonoids have been implicated as a therapy source for many diseases and conditions, including inflammation, vasculitis, [...] Read more.
Flavonoids are a large subgroup of polyphenols known to be sourced from over 6000 natural products, including fruits, vegetables, bark, and herbs. Due to their antioxidant properties, flavonoids have been implicated as a therapy source for many diseases and conditions, including inflammation, vasculitis, venous insufficiency, and hemorrhoids. Currently, some flavonoids are being researched for their antioxidant ability concerning neuroprotection. These flavonoids can penetrate the blood–brain barrier and, depending on the specific flavonoid, retain adequate bioavailability in certain brain regions. Further data suggest that flavonoids could have a strong anti-inflammatory effect in the brain, which not only could be a robust therapeutic source for known neuroinflammatory diseases such as Alzheimer’s Disease or Parkinson’s Disease but also could be a therapeutic source for ischemic or hemorrhagic conditions such as a stroke. While flavonoid toxicity exists, they are relatively safe and non-invasive drugs from natural origins. As such, exploring the known mechanisms and therapies may highlight and establish flavonoid therapy as a viable source of therapy for stroke patients. As stated, many flavonoids are already being isolated, purified, and implemented in both in vitro and in vivo experiments. As these flavonoids proceed to clinical trials, it will be important to understand how they function as a therapy, primarily as antioxidants, and by other secondary mechanisms. This review aims to elucidate those mechanisms and explore the neuroprotective role of flavonoids. Full article
(This article belongs to the Special Issue Cellular and Molecular Basis of Neurodegenerative Disease)
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